Fusarium wilt of cotton, caused by the fungus Fusarium oxysporum Schlechtend. f. sp. vasinfectum (Atk.) Snyd. & Hans, was first identified in 1892 in cotton growing in sandy acid soils in Alabama (8). Although the disease was soon discovered in other major cotton-producing areas, it did not become global until the end of the next century. After its original discovery, Fusarium wilt of cotton was reported in Egypt (1902) (30), India (1908) (60), Tanzania (1954) (110), California (1959) (33), Sudan (1960) (44), Israel (1970) (27), Brazil (1978) (5), China (1981) (17), and Australia (1993) (56). In addition to a worldwide distribution, Fusarium wilt occurs in all four of the domesticated cottons, Gossypium arboretum L., G. barbadense L., G. herbaceum L., and G. hirsutum L. (4,30). Disease losses in cotton are highly variable within a country or region. In severely infested fields planted with susceptible cultivars, yield losses can be high. In California, complete crop losses in individual fields have been observed (R. M. Davis, unpublished). Disease loss estimates prepared by the National Cotton Disease Council indicate losses of over 109,000 bales (227 kg or 500 lb) in the United States in 2004 (12).
Following the discovery of fusarium wilt in Australian cotton crops in 1993, isolates of Fusarium oxysporum f. sp. vasinfectum were collected from 6 cotton farms on the Darling Downs of Queensland. Using a range of procedures the Australian isolates could not be differentiated from each other, but they did differ from foreign isolates of the pathogen in a number of characteristics. Pathogenically, the isolates behaved similarly to race 6 of the pathogen when inoculated onto differential lines. Using aesculin hydrolysis tests, however, it was difficult to match local isolates with any of the known races. Additionally, none of the foreign isolates examined produced detectable volatile compounds when grown on a starch substrate, while all Australian isolates produced a distinctive odour during these tests. The local strain was not vegetatively compatible with any of the foreign isolates and belonged in a single, unique vegetative compatibility group. It is speculated that the Australian strain arose locally, perhaps from a minor population becoming prominent in response to wide-scale planting of highly susceptible cotton cultivars. These findings have significant implications for control of the disease and spread of the pathogen in Australia.
Uredospore survival and the development of soybean rust were examined across a range of temperatures. To determine the effect of temperature on uredospore survival, samples of dry uredospores were exposed to each of a series of eight temperatures for 8 h prior to a germination test on water agar at 21°C for 4 or 16 h. Germination was significantly reduced when uredospores had been exposed to temperatures of 28.5–42.5°C. Development of rust in soybeans was examined under four temperature regimes. Following inoculation with uredospores, plant foliage was sprayed with water and kept under conditions of dew at 21°C for 16 h. Plants were then placed in a selected regime. The 17–27°C regime provided the best conditions for rust development. These findings may partially explain some of the observations on rust occurrence in the field.
Summary. Fusarium wilt, caused by
Fusarium oxysporum f. sp.
vasinfectum, is a new and important disease of cotton in
Australia. Some factors affecting either the infection process or the
subsequent development of symptoms under glasshouse conditions were examined
in this study. The pathogenicity of inocula was significantly affected by the
media in which they were produced. The most severe symptoms developed in the
plants inoculated with the inoculum produced in Komada-Ezuka liquid medium, in
which glucose and L-asparagine were used as the carbon and nitrogen source,
respectively. Symptoms were significantly more severe in plants inoculated
with the inocula suspended in culture filtrates than in those inoculated with
the inocula suspended in distilled water, indicating that fungal metabolites
played an important role in the infection process. The disease was enhanced by
high conidial concentration (>1.0 x 106
conidia/mL), slightly acidic inoculum (pH 4.0–5.5) and longer
inoculation period (5–25 min). One-week-old seedlings were most
susceptible, regardless of cultivar, and the resistance of plants increased
with their age. The development of symptoms was enhanced at a moderate
temperature range (18–23°C), but suppressed at a higher temperature
range (28–33°C). Based on these results, an optimised procedure of
pathogenicity assay is described.
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